Winter ulcer is a known and only partly unsolved problem within the salmonid farming industry, especially relevant for the Atlantic salmon and rainbow trout farming. Winter ulcer causes annual losses of around NOK 100 million to the Norwegian aquaculture industry. In addition new findings show that more than 7 million salmons already vaccinated against winter ulcer are potentially lost to the industry only during the first 3 months after sea transfer due to ulcers that often is demonstrated to be winter ulcer. Industry officials has also identified a substantial lack of reporting of the illness, as the reporting of this disease is not mandatory and required. Out of the NOK 100 million registered losses, NOK 20 million are caused by down-classification of fish products due to scars and damaged muscle tissue which again causes a lowered meat quality.
Winter ulcer has also been a problem to the aquaculture industry in Scotland, Iceland, Faroe Islands, Ireland, Canada and Maine in USA (Bruno et al. 1998, Gudmundsdottir et al. 2006, Whitman et al. 2000).
Moritella viscosa has since long been shown to be causing winter ulcer in farmed salmonid fish. From the first known outbreaks of disease in the 1980s focus has been on preventing and controlling the disease by controlling the bacterium M. viscosa. Since 1993, fish have been vaccinated against winter ulcer, and the main strategy today is to use a multi-component vaccine in vaccination of smolts before sea launch. M. viscosa is one of the up to six microbial components in the multi-component vaccines from all the vaccine producers. The other components than M. viscosa are intended to protect against other diseases than winter ulcer. Vaccination of farmed Atlantic salmon has for nearly three decades been performed with one single intra-peritoneal injection of a multi-component vaccine protecting against up to 6 different infectious diseases before smoltification and sea launch. Since vaccination against winter ulcer started the vaccine effect has not been optimal, being successful with ≧60% relative protection.
From the first known outbreak of winter ulcer in the early 1980s, and throughout the time period to the present, it is well documented that Vibrio wodanis (V. wodanis) is isolated along with M. viscosa from both head kidney and wounds in diseased salmon. It was from the beginning of the 1990s, both in Norway and Iceland documented that M. viscosa could reproduce many of the symptoms seen in winter ulcer by using a healthy salmon in the challenge. Parallel challenge with V. wodanis did not produce any disease. It was employed intramuscular challenge in these early experiments. Hence, it was concluded that V. wodanis did not have any important role in the development of winter ulcer.
Aunsmo et al. in 2008 document ulcers as accounting for 43% of the mortality in Atlantic salmon smelts already vaccinated against winter ulcer during the 3 first months after transfer to sea. It was shown that ulcers occurred in outbreaks with both M. viscosa and V. wodanis isolated from the kidneys of vaccinated but diseased salmon. In addition ulcers occurred as a cause of low baseline mortality during the first 3 months. Further winter ulcer occurs as a problem in all parts of the growth period.
The diseased post-smolts will also have a lower chance of becoming fully grown salmons having a higher mortality rate. The study published by Aunsmo in his 2010 dissertation had followed 2.7 million vaccinated post-smolts after transfer to sea in 20 different cages at 10 different localities in Norway. Overall mortality of the smolts was about 2.5% with the main cause of mortality explained by wounds (mainly winter ulcer) accounting for 43% of deaths in spite of the use of the only relatively effective commercial multi-component vaccine with the winter ulcer component. Extrapolated, 2.5% of the about 280 millions of salmon smolts ‘launched’ in total annually in Norway die from wounds that primarily is caused by winter ulcer the first 3 months after transfer from freshwater to net pens in sea.
Wodanosis as defined herein may produce skin ulcers in combination with septicemia or may be dominated by septicemia in the summer months which may mean that as much as 4-5% of the smolts are lost the first 3 months in sea because of either winter ulcer or wodanosis.
Winter ulcer occurs throughout the complete growth period except for the summer months and the total losses including loss of salmon near to slaughter is not known. However, in 2008 it was reported a direct loss from down-classification of slaughtered salmon of NOK 20 million suspected to be mainly caused by winter ulcer in only one single salmon farm (ref Fiskehelserapporten V I, 2008).
Winter ulcer is a disease not required to report, but by an annual phone call to the local Fish Health Services made by an official at the National Veterinary Institute annually between 35 and 55 farms is “remembered” to have had outbreaks of winter ulcer by the various Fish Health Services. In the fish health report from the National Veterinary Institute covering 2010 it is noted that a “Smolt syndrome” has been recorded just after transfer to sea. The smolts grow poorly and develop ulcers and it is related to improper smoltification in large batches of salmon transferred to unusually cold water. It is reason to believe that winter ulcer bacteria together with Tenacibaculum spp. bacteria may be related to these ulcer problems.
As a result from a collaboration between the vaccine company Alpharma (Pharmaq from 2004) and the Icelandic fish health research scientists at Keldur, University of Iceland, Reykjavik, an autogen vaccine against atypical furunculosis was made in 1991. From 1992 V. wodanis was added to this vaccine against atypical furunculosis because the land-based fish farms in Iceland pumped seawater from relatively large depths that resulted in winter ulcer in the tanks. Possibly because V. wodanis was easier to cultivate than M. viscosa, V. wodanis was chosen for this specially made autogenic vaccine that however did not improve the situation. From 1993 M. viscosa was included as a third component in the vaccine and the occurrence of winter ulcer dropped considerably.
However, after a collective evaluation in 1995 V. wodanis was removed from the vaccine without any increase in the number of outbreaks in the land-based tanks. (Thorarinsson og Lystad, Norsk Fiskeoppdrett, nr 10, 2003).
In 2007 V. wodanis was reclassified as Aliivibrio wodanis (A. wodanis) (WoRMS (2011). Aliivibrio wodanis Lunder, Serum, Holstad, Steigerwalt, Mowinckel & Brenner, 2000. Accessed through: World Register of Marine Species at http://www.marinespecies.org/aphia.php?p=taxdetails&id=570711 on 2012 May 12). The terms A. wodanis and V. wodanis are used as synonyms in this description.
A. wodanis has once previously been included in an experimental vaccine against winter ulcer in Atlantic salmon in a challenge and vaccination study without causing increased protection against winter ulcer (Greger and Goodrich, 1999). In the experiment no pathogenicity was demonstrated by A. wodanis by intraperitoneal injection in rainbow trout and therefore the vaccinated Atlantic salmon were not challenged with A. wodanis. The lack of disease development in rainbow trout at 10° C. after intraperitoneal injection may be caused by fish species specificity or any methodological impact not reported. The vaccinated salmon fry was challenged intraperitoneally with M. viscosa in the study of Greger and Goodrich (1999) and no increased protection against M. viscosa caused after introduction of A. wodanis in the vaccine was reported.
Thorarinsson & Lystad et al (2003), summarized research and field experiences related to the virulence of V. wodanis in winter ulcer, but concluded that it did not have an immediate role in the disease. In addition, it was also mentioned therein using V. wodanis in a vaccine did not provide any protection against winter ulcer.
A specific vaccine tested in the field on Iceland containing A. wodanis did not improve the protection against winter ulcer and A. wodanis was later withdrawn from the vaccine since M. viscosa alone was reported to protect effectively against winter ulcer (Thorarinsson & Lystad et al (2003)).
Greger & Goodrich (1999) also concluded that V. wodanis was not a pathogen. The same conclusion was drawn by Lunder et al. 1995.
Accordingly no virulence in disease has yet been proven for A. wodanis. In addition, no medical use thereof and particularly not a medical use thereof in the form of a functional vaccine has been proven. Furthermore, the role of A. wodanis in winter ulcer has never been clarified, as it has been concluded to be of no use in the development of vaccines for this disease. Hence, the role of V. wodanis in diseases affecting fish remains blurred, and especially its interaction, if any, with M. viscosa. 
In summary, there is a need in the art to overcome or at least mitigate the problems associated with disease in fish, such as Salmonidae, by finding alternative vaccine solutions to the vaccines available as of today. There is a further need in the art for improvements of the vaccines to winter ulcer as well as vaccines for the treatment and/or prevention of the herein defined novel disease, wodanosis. There is a further need in the art for an improved vaccine which will remove most of the loss caused by ulcers in the salmonid farming and also improve the product quality due to the occurrence of reduced scars and connective tissue in the meat of salmon surviving winter ulcer especially in spring and summer when sea water temperatures rise and ulcers heal leaving scars.